In reverse translational studies, rats subjected to 15 days of chronic unpredictable stress (CUS) – a validated rodent model of depression – had a 35% decrease in cellular proliferation in the cingulate, motor, and prelimbic cortices; the selective serotonin reuptake inhibitor (SSRI) fluoxetine reversed this deficit and increased sucrose preference, a surrogate marker of anhedonia (Banasr et al. 2007). Interestingly, this study reported reduced endothelial and oligodendrocyte progenitor proliferation but no change in astrocytes and microglia (Banasr et al. 2007). Chronic social defeat by an aggressive conspecific decreased medial PFC gliogenesis and hippocampal dentate gyrus neurogenesis, but had minimal trophic effects in non-limbic brain structures; again, SSRIs reversed these impairments (Czeh et al. 2007), further suggesting the importance of serotonergic circuitry in astrocyte-mediated dysfunction.
